The effects of post‐exercise glucose and alanine ingestion on plasma carnitine and ketosis in humans.

Abstract

SUMMARY1. Several studies have hypothesized that alanine decreases plasma ketone body levels by increasing availability of oxaloacetate, thus allowing acetyl groups to enter the tricarboxylic acid cycle and releasing co-enzyme A (CoA).2. Four, fasted adult males exercised at 50 % of their maximal oxygen consumption for 1-5 h, then ingested 100 g of either glucose or alanine 2 h into recovery.3. Post-exercise ketosis had developed at 2 h into recovery, as shown by a significantly elevated concentration of ,?-hydroxybutyrate in the plasma. At this time plasma free fatty acids were elevated above resting levels while plasma free carnitine concentrations had fallen below resting values.4. After either alanine or glucose ingestion ,-hydroxybutyrate concentrations fell to the same extent. After the alanine load free carnitine increased above that seen in the glucose trial. Following either alanine or glucose ingestion free fatty acid levels fell; they remained at resting levels in the alanine trial but decreased below rest in the glucose trial.5. We assume that plasma carnitine concentrations largely reflect the hepatic carnitine pools; therefore, elevations in the plasma free carnitine are probably the result of an increased utilization of acetyl CoA. The significant elevation in plasma free carnitine concentration found after alanine ingestion is consistent with the hypothesis that alanine increases the oxidation of acetyl CoA by providing oxaloacetate for the tricarboxylic acid cycle.

Exogenous Ketone Supplements in Athletic Contexts: Past, Present, and Future

“…Similar effects have also been observed after resistance exercise [232,233]. The magnitude and time course of PEK are largely dependent on nutrient intake, that is, attenuated by high CHO feeding and alanine ingestion, and augmented by CHO restriction [181,[234][235][236][237][238][239]. During the post-exercise recovery period, in contrast to the reliance on CHO metabolism during exercise, muscle glycogen resynthesis has a high metabolic priority and is facilitated by an increase in fat oxidation and sparing of CHO sources for energy provision [240][241][242][243].…”

Metabolism of ketone bodies during exercise and training: physiological basis for exogenous supplementation

“…, ; Carlin et al . ) attenuate PEK, but the glucose effect is not seen when glucose is ingested immediately after exercise. Alanine ingestion increases mitochondrial [oxaloacetate] in liver, thereby allowing condensation with Ac‐CoA and diversion away from ketogenesis.…”

Insulin Exposure and Unifying Aging

“…The human serum ALCAR/CAR ratio doubles with 1.5 h of only 50% of the maximal oxygen capability (50% V O 2max ) exercise after a single-day fast [19], but vigorous exercise above the lactate threshold is required for 'rapidly' altering the serum acylCAR/CAR ratio in a fed animal [68]. Sustained moderate aerobic exercise (40-70% of V O 2max ) will create a rising ratio of intramuscular ALCAR and other short acyl chain carnitines (relative to total carnitine) that overflow from muscle tissues to blood only for the period of exercise, in contrast to the longer duration of fasting liver-synthesized ALCAR elevations in CR (fasting) animals.…”

“…[15]. A single-day fast elevates the ALCAR/CAR serum ratio some two-fold higher in both rats [16,17] and humans [18] with a similar doubling occurring for the duration of moderately vigorous exercise [19], in both cases without elevation of total CAR (acylCAR and CAR). Human daily variation in ALCAR/CAR ratio, absent exercise, parallels the daily elevation in free fatty acids of our normal nightly fast [20].…”